Evidence map›Paper›PMID 21303939›Full record

ArticleEndocrinology2011

GPR30 activation opposes estrogen-dependent uterine growth via inhibition of stromal ERK1/2 and estrogen receptor alpha (ERα) phosphorylation signals.

Fei Gao, Xinghong Ma, Alicia B Ostmann, Sanjoy K Das

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  3. Effectiveness effects ofOpen veterinary journal · 2025
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  5. Sex and estradiol effects in the rodent dorsal striatum.The European journal of neuroscience · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. GPER1 and microRNA: Two Players in Breast Cancer Progression.International journal of molecular sciences · 2020
    Review
  14. Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020
    Review
  15. Review
  16. Review
  17. Crosstalk between nuclear and G protein-coupled estrogen receptors.General and comparative endocrinology · 2018
    Review
  18. Estrogen, Angiogenesis, Immunity and Cell Metabolism: Solving the Puzzle.International journal of molecular sciences · 2018
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Fei GaoDivision of Reproductive Sciences, The Perinatal Institute, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.
Xinghong Ma
Alicia B Ostmann
Sanjoy K Das
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

ENVIRONMENTAL TOXINS AND UTERINE GENE EXPRESSIONR01ES007814 · NIEHS · VANDERBILT UNIVERSITY · PI DAS, SANJOY K. · 1997 to 2012
$3.2M
Molecular Signaling in DecidualizationR01HD056044 · NICHD · CINCINNATI CHILDRENS HOSP MED CTR · PI DAS, SANJOY K. · 2009 to 2010
$1.1M
NICHD NIH HHS R01 HD056044NICHD NIH HHS R01 HD56044NIEHS NIH HHS R01 ES007814NIEHS NIH HHS R01 ES07814
6 · The paper itself

Abstract

Although estradiol-17β (E2)-regulated early and late phase uterine responses have been well defined, the molecular mechanisms linking the phases remain poorly understood. We have previously shown that E2-regulated early signals mediate cross talk with estrogen receptor (ER)-α to elicit uterine late growth responses. G protein-coupled receptor (GPR30) has been implicated in early nongenomic signaling mediated by E2, although its role in E2-dependent uterine biology is unclear. Using selective activation of GPR30 by G-1, we show here a new function of GPR30 in regulating early signaling events, including the inhibition of ERK1/2 and ERα (Ser118) phosphorylation signals and perturbation of growth regulation under the direction of E2 in the mouse uterus. We observed that GPR30 primarily localizes in the uterine epithelial cells, and its activation alters gene expression and mediates inhibition of ERK1/2 and ERα (Ser118) phosphorylation signals in the stromal compartment, suggesting a paracrine signaling is involved. Importantly, viral-driven manipulation of GPR30 or pharmacological inhibition of ERK1/2 activation effectively alters E2-dependent uterine growth responses. Overall, GPR30 is a negative regulator of ERα-dependent uterine growth in response to E2. Our work has uncovered a novel GPR30-regulated inhibitory event, which may be physiologically relevant in both normal and pathological situations to negatively balance ERα-dependent uterine growth regulatory functions induced by E2.

Indexed as

AnimalsBlotting, NorthernBlotting, WesternCyclopentanesEstrogen Receptor alphaEstrogensFemaleImmunohistochemistryMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3OvariectomyPhosphorylationQuinolinesReceptors, EstrogenReceptors, G-Protein-Coupled1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanoneCyclopentanesEstrogen Receptor alphaEstrogensGPER1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3QuinolinesReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID21303939
PMCPMC3060628
OpenAlexW2041619394

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.